C hlamydia trachomatis remodels stable microtubules to coordinate G olgi stack recruitment to the chlamydial inclusion surface

Summary C hlamydia trachomatis ( Ctr ), an obligate intracellular bacterium, survives and replicates within a membrane‐bound vacuole, termed the inclusion, which intercepts host exocytic pathways to acquire nutrients. Ctr subverts cellular trafficking pathways from the G olgi by targeting small GTP ases, including Rab proteins, to sustain intracellular bacterial replication; however, the precise mechanisms involved remain incompletely understood. Here, we show that C hlamydia infection in human epithelial cells induces microtubule remodeling, in particular the formation of detyrosinated stable MTs , to recruit G olgi ministacks, but not recycling endosomes, to the inclusion. These stable microtubules show increased resistance to chemically induced depolymerization, and their selective depletion results in reduced bacterial infectivity. R ab6 knockdown reversibly prevented not only G olgi ministack formation but also detyrosinated microtubule association with the inclusion. Our data demonstrate that C hlamydia co‐opts the function of stable microtubules to support its development.